Paramedic Intervention into Fluid, Electrolyte and Acid-Base Disturbances in Renal Failure - Case Study Example

Fluid, Electrolyte and Acid-base Disturbances in Renal Failure Student’s Name Institutional Affiliation Fluid, Electrolyte and Acid-base Disturbances in Renal Failure The kidney is one of the major body organs involved in the regulation of body fluids and electrolytes. The homeostatic control of body fluids and electrolytes occur along the renal tubules in the nephron (Thomson & Macnab, 2009; Kraft, Btaiche, Sacks & Kudsk, 2005). A healthy functioning kidney usually excretes approximately 1500ml of water in addition to surplus electrolytes such as phosphate, potassium, sodium and magnesium (Thomson & Macnab, 2009). Therefore, renal failure, be it acute or chronic, may result in a substantial electrolyte and fluid derangements in the body in addition to acid-base imbalance. Occurrence of Chronic Renal Failure (CRF) CRF or Chronic kidney disease (CKD) can be described as a disease characterized by a decrease in "glomerular filtration rate (GFR) to less" than 60ml/min/1.73m2 for at least three months or a progressive loss in the functionality of the renal system that occurs over at least three months to years (Murpbree & Thelen, 2010). CKD's etiology may be a variety of diseases and factors that include hypertension, cystic kidney diseases, vascular diseases, diabetic kidney disease, recurrent kidney stone disease, tubulointerstitial diseases, glomerular diseases, urinary tract dysfunction or obstruction, unresolved episodes of acute kidney injury and congenital renal defects (Metcalfe, 2007; Nahas & Bello, 2005). Moreover, factors such as nephrotoxins, proteinuria, hyperlipidemia, smoking, systemic hypertension, impaired renal perfusion and hyperphosphatemia can aggravate the progress of CKD (Murpbree & Thelen, 2010). Exposure to the above risk factors drives the progressive destruction and loss of renal function. These factors cause cumulative physical damage to the kidney cells that results in the release of "inflammatory mediators, including cytokines, chemokines and growth factors" (Nahas & Bello, 2005). The latter, most notably transforming growth factor (TGF) beta 1, is a primary activator of intracellular signal transduction pathways in glomerular and tubolointerstitial cells. Initially, these pathways mediate healing of injured renal cells but repeated stimulation caused by persistent exposure to diseases or factors highlighted above ultimately results in progressive tubolointerstitial fibrosis and glomerulosclerosis (Nahas & Bello, 2005). The loss of renal function is initially asymptomatic as the kidney possesses innate activity that enables it to maintain a normal GFR due to compensatory hypertrophy and hyperfiltration in the nephron. However, progressive damage leads to persistent uremic symptoms typical of CKD (Thomas, Kanso & Sedor, 2008). Fluid Imbalance in Renal Failure As CKD progresses, fluid abnormalities begin manifesting as the compensatory mechanisms of the kidney get exhausted. This is common when the GFR falls to lower than 15ml/min/1.73m2 during stages 4-5 of the disease (Kovesdy, 2012). The impact of the “renin-angiotensin-aldosterone system” (RAAS) in fluid balances is blunted by sclerosis and fibrosis of the glomeruli and the tubulointerstitial cells (Wolf & Ruster, 2006). At this stage, the ability of the kidney to dilute or concentrate urine maximally has remarkably decreased, therefore, affecting the kidney's ability to respond to alteration in water intake. The dilution capacity is maintained for longer periods compared to the concentration capacity during the late stages of the disease ultimately resulting in a constant urine osmolality despite variation in water intake (Kovesdy, 2012). These changes are central to fluid overload and hypovolemia experienced in CKD (Thomson & Macnab, 2009). In the early stages of CKD, fluid overload may become apparent after an increased fluid intake either orally or parenterally during fluid therapy but this manifestation is overt in the late stages of the disease. Failure of the kidney to excrete free water and excess sodium results in accumulation of fluid in the intracellular and extracellular spaces resulting in edema and hypertension (Thomson & Macnab, 2009). Electrolyte imbalance in RF The predominant electrolyte changes in CKD especially stage 5 of the disease include hyperphosphatemia, hypocalcemia and hyperkalemia. Hyperphosphatemia occurs due to a decrease in phosphate excretion precipitated by impaired glomerular filtration (Karmarkar & Macnab, 2012). Hyperphosphatemia inhibits formation of active calcitriol resulting in diminished calcium absorption in the intestines leading to hypocalcemia (Thomas, Kanso & Sedor, 2008). At GFR of less than 15 ml/min/1.73m2, potassium excretion is decreased resulting in hyperkalemia (Mahaldar, 2012). Serum sodium concentration may vary depending on the water volumes. Hypernatremia is common in hypovolemic states while hyponatremia – dilutional hyponatremia, is common in water overload or after increased fluid intake (Arrovo, 2008). Table 1: Summary table of electrolyte changes in advanced CKD Electrolyte Changes in advanced CKD Potassium ions Increased Phosphate ions Increased Calcium ions Decreased Sodium ions Increased/decreased Acid-base Imbalances in RF The epitome of acid-base imbalance in end-stage RF is uremic acidosis characterized by an anion gap metabolic acidosis (Cibulka & Racek, 2007). With GFR of below 20 ml/min, a normal anion gap metabolic acidosis is common. The kidney regulates blood pH through excretion of excess H+ and production or reabsorption of hydrogen carbonate ions (Mahalder, 2012). This regulation is effected via transporters present in renal tubular cells that are progressively impaired as CKD advances. Ineffective renal bicarbonate and ammonia buffer system ultimately results in accumulation of acidic hydrogen ions due to inability of the kidney to generate and reabsorb sufficient bicarbonate and form ammonia (NH3) buffer (Cibulka & Racek, 2007). The anion gap is precipitated by accumulation of nonvolatile and organic acids. Below is a flow chart of the occurrence of metabolic acidosis in CKD. Signs and Symptoms of RF In the early stages 1-3 of CKD, there are limited or no symptoms despite a higher creatinine or blood urea nitrogen (Snyder & Pendergraph, 2005). In stages 4-5, GFR is less than 30ml/min/1.73m 2 manifesting as deranged metabolic, endocrine, water and electrolyte disturbances (Nahas & Bello, 2005). Inability of the kidney to concentrate urine as the disease progresses may manifest as nocturia. The earliest signs of uremia in renal failure include anorexia, fatigue, lassitude and a reduction in mental acuity (Snyder & Pendergraph, 2005). Metabolic acidosis in stage 5 of the disease presents with signs such as protein-energy malnutrition as a result of renal loss of proteins and essential amino acids, loss of lean body mass and increasing muscle weakness (Cibulka & Racek, 2007). As the kidney’s capacity to handle water and salt decreases as the disease advances, accumulation of fluid – hypervolemia, may result in pulmonary edema, peripheral edema, and hypertension. The latter may aggravate an already existing hypertension since hypertension is a risk factor for CKD (Arrovo, 2008). Anemia resulting from insufficient synthesis of erythropoietin in a deranged kidney manifests as fatigue, reduced exercise tolerance, impaired immunity and cognitive capacity and development of diseases of the cardiovascular system (Murpbree & Thelen, 2010). Occasionally, inability to excrete urea by the kidney results in accumulation and crystallization of urea on the skin after excretion alongside sweat. This manifests as uremic frost on the skin (Mahaldar, 2012). Paramedic Intervention Patient assessment is among the initial steps when handling patients manifesting with acute exacerbation of RF. The patient's history, a physical assessment, fluid and mental status assessment, and cardiac rhythm are all important in identifying pathologies or problems affecting the patient. Treatment at the pre hospital level may be specific depending on the priority after assessment, but it includes providing oxygen to the patient in addition to establishing an IV access (Middleton & Patel, 2014). Endotracheal intubation may be necessary for patients experiencing respiratory distress in addition to positive pressure ventilation (Ho & Wong, 2006). Carefully controlled IV fluids are applicable to patients with hypotension and dehydration signs. The fluids are provided in small – about 200ml-250ml as the dose is increased appropriately with a frequent assessment of alteration in blood pressure and breath sounds (Middleton & Patel, 2014). The latter is instrumental in assessing for pulmonary edema that may be managed by employing "bi-level positive airways pressure [BiPAP]" (Ho & Wong, 2006). Pharmacologically the patient may be treated using diuretics such as furosemide to relieve any edema. Calcium, insulin, 50% dextrose and bicarbonate can manage hyperkalemia. Dosage of these medication may vary but common adult doses include 25 grams of 50% dextrose, 1 mEq/kg of an 8.4% sodium bicarbonate solution, 10 units of subcutaneous insulin and 8-16mg/kg of calcium chloride (Kraft et al., 2005). However, these management measures only serve to support the patient's vital systems and prompt transport to dialysis centers, or a hospital environment should be facilitated for definitive therapy. Conclusion RF may present as either acute renal failure or CKD. The former may occur superimposed on the latter. Paramedics need to identify and understand the presentation of both conditions to guide appropriate emergency interventions. CKD is a chronic condition that progresses through five stages culminating in end-stage renal failure. The initial first three stages may be asymptomatic, but its symptoms in later stages of the disease may be severe if not rapidly and aptly managed. Such symptoms include acid-base imbalances such as metabolic acidosis, and electrolyte disturbances such as hyperkalemia, hyperphosphatemia, and hypocalcemia. Therefore, the paramedics should carry out blood or urine tests to determine the severity of electrolyte and acid-base disturbances before instituting appropriate therapeutic interventions. While managing such patients, paramedics should prioritize their interventions by following the basic ABC where the airways are attended to first stabilizing them before making sure that the patient is in proper breathing condition and that the circulation is intact (Thim, Krarup, Grove, Rohde & Lafgren, 2012). Prioritization of interventions enables the paramedics to attend to vital patient parameters before normalizing any other dysfunction resulting from the disease. Once the patient has stabilized, transport should be urgently provided to the nearest appropriate hospital for further management in a hospital setup. This may include scheduling the patient for dialysis to restore normal homeostatic physiological state of the body. References Arrovo, A.R. (2008). Electrolyte and acid-base balance disorders in advanced chronic kidney disease. Nefrologia, 28(Suppl 3), 87-93. Cibulka, R. & Racek, J. (2007). Metabolic disorders in patients with chronic kidney failure. Physiological Research, 56, 697-705. Ho, K.M. & Wong, K. (2006). A comparison of continuous and bi-level positive airway pressure non-invasive ventilation in patients with acute cardiogenic pulmonary edema: a meta-analysis. Critical Care, 10(2), 1-8. Karmarkar, S. & Macnab, R. (2012). Fluid and electrolyte problems in renal dysfunction. Anaesthesis & Intensive Care Medicine, 13(7), 332-335. Kovesdy, C.P. (2012). Significance of hypo- and hypernatremia in chronic kidney disease. Nephrology Dialysis Transplant, 27, 891-898. Kraft, M.D., Btaiche, I.F., Sacks, G.S. & Kudsk, K.A. (2005). Treatment of electrolyte disorders in adult patients in the intensive care unit. American Journal Health System Pharmacy, 62, 1663-1682. Mahaldar, A.R. (2012). Acid-base and fluid electrolyte disturbances in chronic kidney disease. Clinical Queries: Nephrology, 1(4), 295-299. Metcalfe, W. (2007). How does early chronic kidney disease progress? Nephrology Dialysis Transplantation, 22(suppl 9), ix26-ix30. 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Chronic kidney disease and its complications. Primary Care. Clinics in Office Practice, 35(2), 329-344. Thomson, H. & Macnab, R. (2009). Fluid and electrolyte problems in renal dysfunction. Anaesthesia & Intensive Care Medicine, 10(6), 289-292. Read More